1. Field of the Invention
The present invention is broadly concerned with a method of immunizing cats against Toxoplasmosis wherein use is made of a live, reproductively deficient mutant of Toxoplasma gondii. More particularly, it is concerned with such a method, and the associated vaccine, wherein the mutant is designated T-263 and has ATCC Accession No. 40615.
2. Description of the Prior Art
Toxoplasmosis is a parasitic disease, and research has indicated that the parasite has a complicated life cycle with the infection spreading to many animals. Oocysts (egg spores) are shed in the feces of domestic cats and certain types of wild cats. Oocysts are then spread by contact with the feces. Flies and cockroaches, which eat feces, can serve as transport agents, contaminating animals which do not directly encounter the cat feces. Mice and birds can be infected either from transport agents, or through direct contact and can then spread the infection to animals which prey on them. Humans can be infected by eating raw or rare meats, or by direct contact with infected cat feces, or contaminated soil.
Toxoplasma infections are quite prevalent, with one-quarter to one-half of the adults in the United States and elsewhere asymptomatically infected. While the presence of Toxoplasma infections has long been known, little was discovered about the transmission of Toxoplasma until the late 1930's and 1940's when Toxoplasmosis was found in newborn babies in the U.S. However, the life cycle of Toxoplasma, and the central role played therein by cats, has now been conclusively established.
The spectrum of human disease due to Toxoplasmosis was characterized by a combination of serologic, immunologic and epidemiological studies, and by isolation of the causative agent, Toxoplasma gondii. In the acute infection where cells are destroyed by rapidly proliferating organisms, there may occur fever, pneumonia, and inflammation of the heart muscle, liver and skin (rash). Toward the end of the period or following a subclinical acute infection, localized or generalized swelling of lymph nodes is observed, especially in women. In newborns infected in utero, a subacute disease picture is typical. In addition to the symptoms of acute Toxoplasmosis mentioned above, meningoencephalitis ("brain fever"), often with hydrocephalus ("water on the brain"), and retinochoroiditis (intraocular inflammation) are important. Most of the mothers who have given birth to infected babies had infections without symptoms.
Thus, Toxoplasmosis deserves special attention because of the serious danger it raises for the unborn human baby. A pregnant woman may have the infection and unknowingly infect the fetus. If not diagnosed and treated in time, her child may be born with permanent brain and eye damage. For this reason, efforts to prevent infection during pregnancy are important.
Inasmuch as domestic cats are important spreaders of Toxoplasma oocysts which are shed in their feces, attempts have been made in the past to immunize domestic cats against oocyst shedding. Generally speaking, prior successful immunizations have required primary infection of cats with Toxoplasmosis, followed by the usual oocyst shedding and a buildup of immunity. However, this manner of immunization generates the very phenomenon sought to be avoided, i.e., oocyst shedding, and as such is deemed deficient. This is especially the case when it is considered that infectious oocysts tend to remain active for a period of months up to a year and a half. Meanwhile, attempts to immunize cats using bradyzoites of oocystless Toxoplasma strains have proven unsuccessful.
A successful approach to immunization of cats is described in U.S. Pat. No. 4,473,548, which involves chemoprophylactic treatment of cats after primary Toxoplasma infection, so as to suppress oocyst shedding while giving immunity. In this procedure, cats are initially infected and thereafter monensin or salinomycin is orally administered for essentially preventing oocyst shedding while permitting immunization to develop in the cats. Although monensin was well accepted by kittens without apparent toxicity, hesitancy existed in using monensin because of occasional toxicity problems which have been described in other animals. Furthermore, human tolerance for monensin has not been investigated, and this constitutes another reason for the lack of acceptance of monensin prophylaxis.
Accordingly, there is a decided need in the art for a method of immunizing cats against Toxoplasmosis which eliminates the problem of fecal oocyst shedding while avoiding use of prophylactic drug treatment.